Evidence map›Paper›PMID 40358417›Full record

ArticleClinical and translational gastroenterology2025

L1 Capsid Protein Expression in HPV-Positive Barrett Metaplasia-Dysplasia-Adenocarcinoma Lesions.

Divya I Vythilingam, Shweta Dutta Gautam, Leonardo D Santos, Wei Xuan, Mohammad Rabiei, Shanmugarajah Rajendra

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Article in Clinical and translational gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Divya I VythilingamGastro-Intestinal Viral Oncology Group, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.
Shweta Dutta GautamGastro-Intestinal Viral Oncology Group, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.
Leonardo D SantosDepartment of Anatomical Pathology, Sydney South West Pathology Service, Liverpool Hospital, Liverpool, Sydney, New South Wales, Australia.
Wei XuanDepartment of Medical Statistics, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.
Mohammad RabieiGastro-Intestinal Viral Oncology Group, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.
Shanmugarajah RajendraGastro-Intestinal Viral Oncology Group, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHuman papillomavirus (HPV) has been associated with a subset of Barrett dysplasia and esophageal adenocarcinoma (EAC). The HPV L1 capsid protein has been closely linked to disease regression and is a prognostic factor in HPV-driven cancers of the cervix and anus.

methodsThus, we investigated L1 protein expression in HPV-positive patients representing the esophageal squamous-Barrett metaplasia-dysplasia-adenocarcinoma sequence. L1 protein immunohistochemical staining was correlated with p16 overexpression and E6/E7 mRNA in situ hybridization.

resultsOf 116 HPV DNA-positive patients ([age range: 19-90, mean [SD], 63.2 [13.5], 88 men and 28 women), 73 (62.9%) were genotype 16, 37 (31.9%) genotype 18, and 6 (5.2%) were genotype 6. L1 staining was identified in 64 individuals: 84.9% (28/33) controls, 94.1% (16/17) Barrett's esophagus, 50% (7/14) low-grade dysplasia, (8/21) 38.1% high-grade dysplasia, and 16.1% (5/31) EAC (adjusted P < 0.0001). Conversely, p16 was present in 9.1% (3/33) of controls, 17.7% (3/17) Barrett's esophagus, 57.1% (8/14) low-grade dysplasia, 61.9% (13/21) high-grade dysplasia, and 64.5% (20/31) of EAC patients ( P < 0.0001). Corresponding figures for E6/E7 mRNA positivity was 6.1% (2/33), 23.5% (4/17), 28.6% (4/14), 38.1% (8/21), and 45.2% (14/31), respectively ( P = 0.008). Expression of HPV-L1 and p16 or L1 and E6/E7 mRNA was largely mutually exclusive. DISCUSSION: HPV L1 capsid expression is incrementally lost with increasing esophageal disease severity as in viral-driven anal and cervical lesions. Utility of L1 alone or in combination with p16 and or E6/E7 mRNA in stratifying HPV-positive patients for treatment should be explored in a prospective longitudinal investigation.

Indexed as

AdenocarcinomaBarrett EsophagusCapsid ProteinsEsophageal NeoplasmsOncogene Proteins, ViralPapillomavirus InfectionsAdultAgedAged, 80 and overCyclin-Dependent Kinase Inhibitor p16EsophagusFemaleHumansImmunohistochemistryIn Situ HybridizationMaleCapsid ProteinsCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16E6 protein, Human papillomavirus type 16HPV L1 protein, Human papillomavirusOncogene Proteins, ViralRepressor ProteinsRNA, MessengerBarrett's esophagusdysplasiaesophageal adenocarcinomahuman papillomavirus

Identifiers

PMID40358417
PMCPMC12330356

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